Inhibitory Effects of Baicalin on Ultraviolet B-Induced Photo-Damage in Keratinocyte Cell Line

2008 ◽  
Vol 36 (04) ◽  
pp. 745-760 ◽  
Author(s):  
Wei Min ◽  
Xiang-Fei Lin ◽  
Xu Miao ◽  
Bao-Tao Wang ◽  
Zi-Liang Yang ◽  
...  
Keyword(s):  
Clinical Medicine ◽  
Protein A ◽  
Inhibitory Effect ◽  
Ultraviolet B ◽  
Nuclear Antigen ◽  
Skin Damage ◽  
Protein Levels ◽  
Initial Event ◽  
Pyrimidine Dimers ◽  
Photo Damage

Baicalin, one kind of Chinese herbal medicine with anti-inflammatory and anti-oxidant property, has been commonly used as a clinical medicine. However, little has been known about the effects of Baicalin on ultraviolet (UV) induced photo-aging and photo-carcinogenesis. The photoproduct is critical to the initial event of UV-induced photo-carcinogenesis. The purpose of the present study was to investigate whether Baicalin, in immortalized human keratinocyte HaCaT cells, could inhibit ultraviolet-B (UVB) induced skin damage and its possible underlying mechanisms, such as inhibiting UVB-induced cytotoxicity and apoptosis, cyclobutane pyrimidine dimers (CPDs), down-regulating the expression of regulatory proteins which are related to cell apoptosis and DNA damage/repair. Our study revealed that Baicalin treatment could inhibit the UVB-induced cytotoxicity, apoptosis and CPD level. It also decreased the mRNA expression of apoptosis-regulatory genes (p53-p21 and c-fos), the protein levels of p53, proliferating cell nuclear antigen (PCNA) and repair protein A (RPA), and the secretion of cytokines [interleukin(IL)-6 and tumor necrosis factor (TNF-α)]. These results suggested that Baicalin may have an inhibitory effect on the UVB-induced photo-damage by blocking the relevant cytokine secretion and expression of p53-p21, c-fos, PCNA and RPA genes.

Effect of Epigallocatechingallate on Ultraviolet B-Induced Photo-Damage in Keratinocyte Cell Line

2006 ◽  
Vol 34 (05) ◽  
pp. 911-922 ◽  
Author(s):  
Dan Luo ◽  
Wei Min ◽  
Xiang-Fei Lin ◽  
Di Wu ◽  
Yang Xu ◽  
...  
Keyword(s):  
Regulatory Gene ◽  
Inhibitory Effect ◽  
Ultraviolet B ◽  
Skin Damage ◽  
Protective Mechanisms ◽  
Egcg Treatment ◽  
Keratinocyte Cell ◽  
Cellular Apoptosis ◽  
Anti Oxidant ◽  
Photo Damage

One type of traditional Chinese medicines, epigallocatechingallate (EGCG) has been commonly used as a clinical and skin health protective ingredient. It has been known to have photo-protective, anti-inflammatory, and anti-oxidant effects. However, little is known about the mechanisms of EGCG on UV-induced photo-aging and photo-carcinogenesis. In the present study, we investigated the photo-protective mechanisms of EGCG on UVB-induced skin damage, including the potency of EGCG to inhibit the UVB-induced cytotoxicity, secretion of cytokine (IL-6 and TNF-α), cellular apoptosis, expression of apoptosis-regulatory genes (p53–p21) and c-fos gene in cultured immortalized human keratinocyte HaCaT cells. EGCG treatment decreased UVB- induced cell cytotoxicity and apoptosis. It also inhibited the mRNA expressions of apoptosis-regulatory gene (p53 and p21) and c-fos gene. These results suggest that EGCG may have an inhibitory effect on UVB-induced photo-damage and apoptosis by blocking the cytokine secretion and the mRNA expressions of p53, p21 and c-fos genes.

Repeated exposures of human skin equivalent to low doses of ultraviolet-B radiation lead to changes in cellular functions and accumulation of cyclobutane pyrimidine dimers

2001 ◽  
Vol 79 (4) ◽  
pp. 507-515 ◽  
Author(s):  
Nadine Chouinard ◽  
Jean-Philippe Therrien ◽  
David L Mitchell ◽  
Marielle Robert ◽  
Régen Drouin ◽  
...  
Keyword(s):  
Dna Damage ◽  
Repeated Exposure ◽  
Ultraviolet B ◽  
Skin Equivalent ◽  
Basal Cells ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Cyclobutane Pyrimidine Dimers ◽  
Biochemical Alterations ◽  
Pyrimidine Dimers

Chronic exposure to sunlight may induce skin damage such as photoaging and photocarcinogenesis. These harmful effects are mostly caused by ultraviolet-B (UVB) rays. Yet, less is known about the contribution of low UVB doses to skin damage. The aim of this study was to determine the tissue changes induced by repeated exposure to a suberythemal dose of UVB radiation. Human keratinocytes in monolayer cultures and in skin equivalent were irradiated daily with 8 mJ/cm2 of UVB. Then structural, ultrastructural, and biochemical alterations were evaluated. The results show that exposure to UVB led to a generalized destabilization of the epidermis structure. In irradiated skin equivalents, keratinocytes displayed differentiated morphology and a reduced capacity to proliferate. Ultrastructural analysis revealed, not only unusual aggregation of intermediate filaments, but also disorganized desmosomes and larger mitochondria in basal cells. UVB irradiation also induced the secretion of metalloproteinase-9, which may be responsible for degradation of type IV collagen at the basement membrane. DNA damage analysis showed that both single and repeated exposure to UVB led to formation of (6–4) photoproducts and cyclobutane pyrimidine dimers. Although the (6–4) photoproducts were repaired within 24 h after irradiation, cyclobutane pyrimidine dimers accumulated over the course of the experiment. These studies demonstrate that, even at a suberythemal dose, repeated exposure to UVB causes significant functional and molecular damage to keratinocytes, which might eventually predispose to skin cancer.Key words: UVB, keratinocytes, skin structure, DNA damage, photoproducts.

scholarly journals Antioxidant and Anti-inflammatory Effects of Fermented Eggplant Fruit Extracts with Leuconostoc mesenteroides KD20

2021 ◽  
Vol 27 (5) ◽  
pp. 1278-1285
Author(s):  
Bum-Chun Lee ◽  
Hee-Sook Kim
Keyword(s):  
Leuconostoc Mesenteroides ◽  
Inhibitory Effect ◽  
Ultraviolet B ◽  
Fermented Foods ◽  
Skin Protection ◽  
Skin Damage ◽  
Fruit Extract ◽  
Protection Effect ◽  
Ultraviolet Ray ◽  
Traditional Fermented Foods

We isolated Leuconostoc mesenteroides KD20, which has its application as a cosmetic material, while searching for useful microbes in Gangwon-do’s traditional fermented foods. Eggplant fruit extract (EG) was fermented with lactic acid bacteria L. mesenteroides. HPLC analysis results for the component analysis of EG and the fermented eggplant fruit extract (FEG) showed bio-conversion of quercetin 3-O-β-D-glucoside and rutin. To investigate skin protection effects of EG and FEG against skin damage by ultraviolet ray, we measured antioxidation and inhibitory effect of inflammation-related cytokines in keratinocytes irradiated with ultraviolet B (UVB). Biosynthesis of IL- 1α, which is increased with UVB in keratinocytes, was inhibited by 24.7% and 28.3% at 100 μg/ml of EG and FEG, respectively. Biosynthesis of PGE2 in keratinocytes was inhibited by 45.7% and 52.3% at 100 μg/ml of EG and FEG, respectively, indicating a greater effect of FEG. Therefore, EG and FEG can be used as an excellent material for cosmetics with skin protection effect against ultraviolet irradiation in keratinocytes.

MicroRNA-16-5p Aggravates Myocardial Infarction Injury by Targeting the Expression of Insulin Receptor Substrates 1 and Mediating Myocardial Apoptosis and Angiogenesis

2020 ◽  
Vol 17 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Xiancan Wang ◽  
Yuqiang Shang ◽  
Shilin Dai ◽  
Wei Wu ◽  
Fan Yi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Viability ◽  
Insulin Receptor ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Nuclear Antigen ◽  
Minichromosome Maintenance ◽  
Protein Levels ◽  
Insulin Receptor Substrates ◽  
Creatine Kinase Mb

Purpose: Myocardial infarction is a common cardiovascular disease. MicroRNA-16-5p (miR-16-5p) was upregulated in heart and kidney hypoxia/reoxygenation (H/R) injury. However, the role of miR-16-5p in myocardial infarction injury is still unclear. Methods: Human adult ventricular cardiomyocytes (AC16) were treated with ischemia/reperfusion (H/R). The miR-16-5p level was evaluated through real-time PCR. The activity of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) was detected via LDH and CK-MB monitoring kits. Cell viability was examined with 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetra-zolium bromide (MTT) assay. Western blotting was used to analyze the protein levels. The luci-ferase report assay confirmed the relative luciferase activity. Results: miR-16-5p was elevated in H/R-treated AC16 cells. miR-16-5p overexpression and knockdown were carried out. miR-16-5p knockdown repressed cell apoptosis, attenuated LDH and CK-MB activities, and enhanced cell viability in H/R-treated AC16 cells. Moreover, miR-16-5p knockdown promoted angiogenesis in human microvascular endothelial cells (HMVEC), causing elevation of vascular endothelial growth factor (VEGF), insulin receptor substrates 1 (IRS1), minichromosome maintenance complex component 2 (MCM2) and proliferating cell nuclear antigen (PCNA) protein levels. Moreover, miR-16-5p was testified to target IRS1. IRS1 silencing alleviated miR-16-5p knockdown-mediated inhibition of apoptosis in AC16 cells. Conclusion: miR-16-5p knockdown increased cell viability and angiogenesis, as well as inhibited cell apoptosis by increasing IRS1. These findings indicated that miR-16-5p knockdown may be a new therapeutic target for myocardial infarction.

scholarly journals CK2 Pro-Survival Role in Prostate Cancer Is Mediated via Maintenance and Promotion of Androgen Receptor and NFκB p65 Expression

2019 ◽  
Vol 12 (2) ◽  
pp. 89
Author(s):  
Janeen H. Trembley ◽  
Betsy T. Kren ◽  
Md. J. Abedin ◽  
Daniel P. Shaughnessy ◽  
Yingming Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Inhibitory Effect ◽  
Strongly Correlated ◽  
Protein Levels ◽  
Small Molecule Inhibition ◽  
Prostate Cells ◽  
Cell Death Response ◽  
Stress Signals ◽  
Castrate Resistant

The prosurvival protein kinase CK2, androgen receptor (AR), and nuclear factor kappa B (NFκB) interact in the function of prostate cells, and there is evidence of crosstalk between these signals in the pathobiology of prostate cancer (PCa). As CK2 is elevated in PCa, and AR and NFκB are involved in the development and progression of prostate cancer, we investigated their interaction in benign and malignant prostate cells in the presence of altered CK2 expression. Our results show that elevation of CK2 levels caused increased levels of AR and NFκB p65 in prostate cells of different phenotypes. Analysis of TCGA PCa data indicated that AR and CK2α RNA expression are strongly correlated. Small molecule inhibition or molecular down-regulation of CK2 caused reduction in AR mRNA expression and protein levels in PCa cells and in orthotopic xenograft tumors by various pathways. Among these, regulation of AR protein stability plays a unifying role in CK2 maintenance of AR protein levels. Our results show induction of various endoplasmic reticulum stress signals after CK2 inhibition, which may play a role in the PCa cell death response. Of note, CK2 inhibition caused loss of cell viability in both parental and enzalutamide-resistant castrate-resistant PCa cells. The present work elucidates the specific link of CK2 to the pathogenesis of PCa in association with AR and NFκB expression; further, the observation that inhibition of CK2 can exert a growth inhibitory effect on therapy-resistant PCa cells emphasizes the potential utility of CK2 inhibition in patients who are on enzalutamide treatment for advanced cancer.

scholarly journals Surfactant protein A reduces TLR4 and inflammatory cytokine mRNA levels in neonatal mouse ileum

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lidan Liu ◽  
Chaim Z. Aron ◽  
Cullen M. Grable ◽  
Adrian Robles ◽  
Xiangli Liu ◽  
...  
Keyword(s):  
Proinflammatory Cytokine ◽  
Inflammatory Cytokine ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Mrna Levels ◽  
Wild Type ◽  
Cytokine Mrna ◽  
Protein Levels ◽  
Cytokine Levels

AbstractLevels of intestinal toll-like receptor 4 (TLR4) impact inflammation in the neonatal gastrointestinal tract. While surfactant protein A (SP-A) is known to regulate TLR4 in the lung, it also reduces intestinal damage, TLR4 and inflammation in an experimental model of necrotizing enterocolitis (NEC) in neonatal rats. We hypothesized that SP-A-deficient (SP-A−/−) mice have increased ileal TLR4 and inflammatory cytokine levels compared to wild type mice, impacting intestinal physiology. We found that ileal TLR4 and proinflammatory cytokine levels were significantly higher in infant SP-A−/− mice compared to wild type mice. Gavage of neonatal SP-A−/− mice with purified SP-A reduced ileal TLR4 protein levels. SP-A reduced expression of TLR4 and proinflammatory cytokines in normal human intestinal epithelial cells (FHs74int), suggesting a direct effect. However, incubation of gastrointestinal cell lines with proteasome inhibitors did not abrogate the effect of SP-A on TLR4 protein levels, suggesting that proteasomal degradation is not involved. In a mouse model of experimental NEC, SP-A−/− mice were more susceptible to intestinal stress resembling NEC, while gavage with SP-A significantly decreased ileal damage, TLR4 and proinflammatory cytokine mRNA levels. Our data suggests that SP-A has an extrapulmonary role in the intestinal health of neonatal mice by modulating TLR4 and proinflammatory cytokines mRNA expression in intestinal epithelium.

scholarly journals UVB protective effects of Sargassum horneri through the regulation of Nrf2 mediated antioxidant mechanism

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Eui Jeong Han ◽  
Seo-Young Kim ◽  
Hee-Jin Han ◽  
Hyun-Soo Kim ◽  
Kil-Nam Kim ◽  
...  
Keyword(s):  
Skin Barrier ◽  
Human Keratinocytes ◽  
Underlying Mechanism ◽  
Ultraviolet B ◽  
Sargassum Horneri ◽  
Cellular Damage ◽  
Protective Effects ◽  
Skin Damage ◽  
Antioxidant Mechanism ◽  
Induced Apoptosis

AbstractThe present study aimed to evaluate the protective effect of a methanol extract of Sargassum horneri (SHM), which contains 6-hydroxy-4,4,7a-trimethyl-5,6,7,7a-tetrahydrobenzofuran-2(4H)-one (HTT) and apo-9′-fucoxanthinone, against ultraviolet B (UVB)-induced cellular damage in human keratinocytes and its underlying mechanism. SHM significantly improved cell viability of UVB-exposed human keratinocytes by reducing the generation of intracellular reactive oxygen species (ROS). Moreover, SHM inhibited UVB exposure-induced apoptosis by reducing the formation of apoptotic bodies and the populations of the sub-G1 hypodiploid cells and the early apoptotic cells by modulating the expression of the anti- and pro-apoptotic molecules, Bcl-2 and Bax, respectively. Furthermore, SHM inhibited NF-κB p65 activation by inducing the activation of Nrf2/HO-1 signaling. The cytoprotective and antiapoptotic activities of SHM are abolished by the inhibition of HO-1 signaling. In further study, SHM restored the skin dryness and skin barrier disruption in UVB-exposed human keratinocytes. Based to these results, our study suggests that SHM protects the cells against UVB-induced cellular damages through the Nrf2/HO-1/NF-κB p65 signaling pathway and may be potentially useful for the prevention of UVB-induced skin damage.

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